Rh Disease – Sweet, Sweet Blood Cells – Part 1

… and, we’re back! Grad school and life kept me pretty busy in the last year. The Ebola and Disneyland measles outbreaks almost roused me into writing a post, but it was an article on Rh disease that finally did it.

Do you know your blood type? I… don’t actually know mine. Barring emergency circumstances, most people first become acquainted with the complications of blood type when they have a baby. Certain mothers who are Rh- (“R h negative”) need shots during their pregnancy to protect their next baby. Which mothers? Why do they need shots? Why is it for the next baby? Let’s dive in!

The most important sugars we call A and B, from which we get the blood types A, B, AB, and O (O means simply the absence of A and B). The types of sugars on your RBCs determine your blood type.

Blood type is determined by which sugars are on your red blood cells: A sugars, B sugars, both (AB), or none (O).

The next most important blood sugar is the Rhesus D sugar2, abbreviated RhD or simply Rh. If you have this sugar, your blood type is Rh+; otherwise, you’re Rh-. Jill is type B and Rh-, so we just say B-.

Sometimes, a person makes antibodies against sugars she doesn’t have. An antibody is a Y-shaped protein that makes a strong bond to one particular substance like a key in a lock. These antibodies swim through the bloodstream looking for invading cells that they can tag and destroy.3

Antibodies tag an invader for destruction.

If Jill (type B) gets a transfusion from Jack (type A), her body recognizes the A sugars as foreign and destroys his RBCs. She now doesn’t get the RBCs she needed, but she also has to deal with getting rid of all the destroyed cell garbage.

So, blood types are determined by sugars, and your body destroys blood with the wrong sugars.

Sensitization

But why do we destroy foreign RBCs? Where do these antibodies come from? We’re not born with them – they develop through a process called sensitization.

Certain white blood cells (WBCs) start life producing one type of antibody, like a key attached to the cell. Before the WBC is allowed out into the world, Jill’s body checks to make sure that the key doesn’t fit into locks on any of Jill’s own cells. If the key fits, the cell is killed. That’s why Jill, with type B blood, doesn’t have any anti-B antibodies.

Before this WBC can be released into the blood, it must pass the test: does its key, meant to detect invaders, bind with anything of Jill’s?

After passing that test, surviving WBCs roam the blood looking for a lock that fits their key. If the cell finds a matching lock, it produces a ton of free-floating key antibodies ready to destroy the next lock they see.4

Sugars that look like A and B actually appear all over nature, so your body sees those “locks” when you eat food. Jill’s body once saw an A sugar on something she ate, and her WBC produced a lot of anti-A antibodies that will stick with her as defenders for life.5

The RhD sugar is pretty rare in nature, so the only way to get antibodies against it is to see RhD+ blood. Unless your WBCs have seen RhD+ blood, you don’t have anti-RhD antibodies.

Hemolytic Disease of the Newborn

Jill’s blood type is B-. Say she gets pregnant for the first time with a baby whose blood type is B+ (congratulations!). As we learned in Fetal Circulation, throughout a normal pregnancy, mom’s blood and baby’s blood never mix. So, Jill’s WBCs never see the RhD sugar and thus never produce antibodies against it.

Until: birth. During childbirth, it is common for up to 1 mL6 of baby’s blood to enter mom’s bloodstream.7 As baby’s RhD+ blood cells circulate, mom is on the lookout for invaders.

Uh oh! Jill’s body thinks that baby’s RhD+ cell is an invader.

Found one! Mom’s WBC latches on to the RhD sugar and starts to produce antibodies against it (anti-RhD antibodies). Long after baby’s blood is cleared from her system, mom’s antibodies will continue to look out for any invading RhD sugars. These antibodies aren’t produced until the birth of Jill’s first baby, so this baby has no problems.

Down the road, Jill gets pregnant again, with another B+ baby (congratulations!). Unfortunately, Jill’s body is on the lookout for the invaders it met when big sister was born. Though Jill’s WBCs are too big to pass through the placenta, her antibodies aren’t.

For the most part, mom’s antibodies going to baby is a good thing. They help protect baby against some diseases until baby can do it himself. Unfortunately, the anti-RhD antibodies aren’t there to be helpful. They latch on to baby’s RBCs and mark them for destruction. This problem is called hemolytic (“blood breaking-open”) disease of the newborn.

Most maternal antibodies are helpful, but the anti-D antibodies mark baby’s RBCs for destruction.

What happens to baby?

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Sources and Further Reading

I’m fairly certain you need your own plush red blood cell; I have one on my desk. Help support Pathology Storybook by using this affiliate link!

Actually, there’s a long process by which this cell alerts another WBC which activates another WBC which then produces a ton of antibodies, but we’ll keep it simple. [↩]

The antibodies themselves actually only last about 20 days, but Jill’s body will continue to produce antibodies because it continues to see the invading sugar. When a body clears an invading agent, like the flu (See our previous post!), some WBCs will become memory cells. These WBCs live a long time and enable fast production of antibodies if that particular strain ever invades again. [↩]